Angiopoietin-Like 8 Governs Osteoblast-Adipocyte Lineage Commitment During Skeletal Aging
As we age, our bones often become weaker, a condition known as osteoporosis. A key factor contributing to this is a shift in how stem cells in our bone marrow develop. Normally, these versatile cells can turn into various cell types, including bone-building cells (osteoblasts) and fat cells (adipocytes). However, with aging, these stem cells tend to produce more fat cells and fewer bone cells, leading to weaker bones and an increase in fat within the bone marrow.
Recent research has shed light on a protein, Angiopoietin-like 8 (ANGPTL8), as a critical player in this age-related imbalance. This protein, which is also involved in how our bodies handle fats, was found to “steer” bone marrow stem cells towards becoming fat cells rather than bone cells. When levels of this protein were elevated in mice, they showed reduced bone mass and more fat in their bone marrow. Conversely, reducing the activity of this protein led to less bone loss and less fat accumulation in the bone marrow. The study also revealed that this protein exerts its influence by interfering with a crucial cellular communication pathway called Wnt/β-catenin signaling, which is essential for bone formation.
These findings suggest that targeting this protein could be a promising strategy to combat age-related bone deterioration. Indeed, treatment with a special molecule designed to block the protein’s activity significantly improved the bone health in aging mice. Understanding this mechanism opens new avenues for developing treatments to maintain bone strength as we get older.